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102. Deficiency in Bhlhe40 impairs resistance toH. polygyrus bakeriand reveals novel Csf2rb-dependent regulation of anti-helminth immunity

103. A Stem-Cell-Derived Platform Enables Complete Cryptosporidium Development In Vitro and Genetic Tractability

104. Challenges in IBD Research: Preclinical Human IBD Mechanisms

109. Ileal Gene Expression Data from Crohn’s Disease Small Bowel Resections Indicate Distinct Clinical Subgroups

110. PAI-1 augments mucosal damage in colitis

113. Forward Genetics in Cryptosporidium Enabled by Complete in Vitro Development in Stem Cell-Derived Intestinal Epithelium

116. Interaction between smoking and ATG16L1T300A triggers Paneth cell defects in Crohn’s disease

117. Atg14 protects the intestinal epithelium from TNF-triggered villus atrophy.

118. Survival signal REG3α prevents crypt apoptosis to control acute gastrointestinal graft-versus-host disease

119. Temporal Regulation of the Bacterial Metabolite Deoxycholate during Colonic Repair Is Critical for Crypt Regeneration

122. A Common Mechanism Links Activities of Butyrate in the Colon

123. Regenerating Islet-Derived 3-Alpha (REG3A) Protects the Intestinal Stem Cell Niche to Control Acute Gastrointestinal Graft-Versus-Host Disease

125. P109 SMOKING NEGATIVELY AFFECTS DISEASE COURSE REGARDLESS OF SMOKING AMOUNT AND MAY BE ASSOCIATED WITH PANETH CELL PHENOTYPE IN JAPANESE CROHN’S DISEASE PATIENTS

131. Helicobacter species are potent drivers of colonic T cell responses in homeostasis and inflammation

132. Dichotomous Effects of ATG16L1 and LRRK2 in Modulating Paneth Cell Defect in Japanese and North American Crohn's Disease Patients

135. LRRK2 but not ATG16L1 is associated with Paneth cell defect in Japanese Crohn’s disease patients

137. A Dietary Fiber-Deprived Gut Microbiota Degrades the Colonic Mucus Barrier and Enhances Pathogen Susceptibility

140. Paneth cell defects in Crohn’s disease patients promote dysbiosis

147. Runx3 specifies lineage commitment of innate lymphoid cells

150. Colitogenic Bacteroides thetaiotaomicron Antigens Access Host Immune Cells in a Sulfatase-Dependent Manner via Outer Membrane Vesicles

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